Low-voltage-activated persistent inward calcium currents (Ca PICs) occur in rat motoneurons, and are mediated by Cav1.3 L-type calcium channels (L-Ca current). The objectives of this paper were to determine if this L-Ca current activates a sustained calcium-activated potassium current (SK current) and examine how such SK currents change with spinal injury. For comparison, the SK current that produces the post-spike afterhyperpolarization (mAHP) was also quantified. Intracellular recordings were made from motoneurons of adult acute and chronic spinal rats while the whole sacrocaudal spinal cord was maintained in vitro. Spikes/AHPs were evoked with current injection or ventral root stimulation. Application of the SK channel blocker apamin completely eliminated the mAHP, which was not significantly different in chronic and acute spinal rats. The Ca PICs were measured with slow voltage ramps (or steps), with tetrodotoxin to block sodium currents. In chronic spinal rats, the PICs were activated at -58.6 ± 6.0 mV and were 2.2 ± 1.2 nA in amplitude, significantly larger than in acute spinal rats. Apamin significantly increased the PIC, indicating that there was an SK current activated by L-Ca currents (SKL current), which ultimately reduced the net PIC. This SK_L current was not different in acute and chronic spinal rats. The SK_AHP and the SK_L currents were activated by different calcium currents because the mAHP/ SK_AHP was blocked by the N, P-type calcium channel blocker -conotoxin MVIIC and was resistant to the L-type calcium channel blocker nimodipine, whereas the L-Ca and SK_L currents were blocked by nimodipine.